Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine serum thyroxine-binding globulin (TBG) levels, we used radioimmunoassay, and compared the results obtained with other tests in 231 patients with chronic hepatitis B virus infection to evaluate its clinical implications. All of these patients were hepatitis B surface antigen (HBsAg)-positive. Among them, 38 patients had hepatocellular carcinoma (HCC), 18 had chronic persistent hepatitis, 70 had chronic lobular or active hepatitis (grouped as CAH), 31 had active cirrhosis (AC), 25 had inactive cirrhosis, 20 had decompensated cirrhosis, and 29 were "healthy" HBsAg carriers. Twenty-seven patients with acute hepatitis, 12 with cancer metastasis to the liver, and 81 normal adults served as disease or normal controls. The results showed that serum TBG level increased significantly in patients with CAH, AC, or HCC. Serum TBG did not correlate with albumin or bilirubin level, but correlated with alanine aminotransferase (ALT) positively in patients with CAH (p less than 0.001) and negatively in patients with HCC (p less than 0.01) (slope difference p less than 0.05). Serial determination of serum TBG and ALT also showed parallel changes in 15 patients with CAH, but not in nine patients with HCC. In contrast, the fall and rise of serum TBG levels in patients with HCC coincided with tumor resection and recurrence. The data suggest that serum TBG elevation in patients with hepatitis activity is the result of hepatocellular damage, whereas that in patients with HCC is due to increased synthesis. Whether serum TBG elevation without concomitant rise of ALT could be used as a marker of HCC awaits further study.
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PMID:Thyroxine-binding globulin in patients with chronic hepatitis B virus infection: different implications in hepatitis and hepatocellular carcinoma. 168 51

Thyroid function tests were evaluated in 34 patients with acute viral hepatitis (AVH) and in 38 healthy controls (C). As expected, AVH patients displayed a significant increase in T4, rT3 and TBG serum levels with respect to C, while FT4 and TSH concentrations were similar. A positive correlation between TBG and T4 was evident in C, but not in AVH. In this group there was, instead, an inverse correlation between the sum of serum levels of GOT + GPT and T4 concentrations. When AVH patients were divided in "high necrosis" (HN, serum GOT + GPT greater than 2000 UI/l) and "low necrosis" (LN, serum GOT + GPT less than 2000 UI/ml) groups, we found a significant reduction in both T4 and T3 serum concentrations in HN with respect to LN, despite similar levels of TBG, albumin, FT4 and TSH. The hypothesis that thyroid-hormone binding inhibitors (THBI), released during severe liver cell injury, accounted for an impaired serum binding capacity in HN-AVH, was confirmed by the significant increase in FT4/T4 ratio and by the demonstration of THBI activity in pooled sera of these patients, with respect to LN subgroup. Our present finding may clarify the unexplained observation of reduced T4 levels in patients with fulminant hepatitis and the ominous prognostic significance of a "low T4 syndrome" in subjects with severe liver disease and/or other systemic illnesses.
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PMID:Thyroid function tests in acute viral hepatitis: relative reduction in serum thyroxine levels due to T4-TBG binding inhibitors in patients with severe liver cell necrosis. 249 20

To evaluate thyroid function in 19 patients with fulminant hepatitis (FH), we have measured total and free 3,5,3'-triiodothyronine (T3) and thyroxine (T4), 3,3',5'-triiodothyronine (reverse T3, rT3), thyroid-stimulating hormone (TSH) and thyroxin-binding globulin (TBG) in patients with FH, compared with those of 80 patients with other various liver diseases and of 10 healthy controls. Patients with FH showed the lowest values of serum T3 and the highest levels of rT3 among all patients with liver diseases studied. Furthermore, patients with FH showed a significant increase of rT3 in comparison with subacute hepatitis (SAH), "acute-on-chronic" (AOC) type of hepatic failure, ordinary and severe forms of acute hepatitis (AHo and AHs) and decompensated liver cirrhosis (LC-D). In addition, serum T3 and rT3 and the rT3/T3 ratio significantly correlated with prothrombin time (PT) and plasma methionine level. We also found that serum T3 and rT3 concentrations and the rT3/T3 ratio showed early and rapid normalization in cases of FH that survived, but they did not improve in patients with fatal outcome. These results suggest that serum T3, particularly rT3 concentrations and the rT3/T3 ratio may be useful indicators for assessing the severity and prognosis of patients with FH and can be considered to the sensitive indices for functioning hepatic microsomal reserve as well.
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PMID:Serum thyroid hormone levels in patients with fulminant hepatitis: usefulness of rT3 and the rT3/T3 ratio as prognostic indices. 311 36

T4-binding globulin (TBG), a glycoprotein with four N-glycosyl complex oligosaccharide chains, exhibits sialic acid-dependent microheterogeneity on isoelectric focusing (IEF). Increasing the sialic acid content of TBG increases its anodal IEF mobility and decreases its rate of in vivo degradation, a mechanism for the elevation of serum TBG levels in pregnancy. In this study, the structure of oligosaccharides in TBG from subjects with various conditions associated with TBG excess was determined by measuring the proportion that bound to Concanavalin-A (Con-A). Since oligosaccharides with three or more branches (antennae) attached to the trimannosyl core are excluded from binding to Con-A, the percentage of serum TBG not bound to Con-A (% peak A) represented the portion of TBG molecules with three or more antennae in all oligosaccharide chains interacting with Con-A. Peak A contained the most anodal IEF bands, while the Con-A-bound TBG (peak B) contained the cathodal bands. Serum samples from 10 normal men and 10 premenopausal women did not significantly differ in terms of TBG levels, % peak A, or IEF mobility and were combined as a single group (normal). Eight subjects with elevated serum TBG levels due to inherited TBG excess [62.0 +/- 10.1 (+/- SD) mg/L] or 2 receiving 5-fluorouracil treatment (26.2 and 31.3 mg/L) compared to 20 normal (14.7 +/- 3.3 mg/L) had % peak A values and IEF mobility similar to those in normal subjects. On the other hand, high serum TBG levels in 8 women during the third trimester of pregnancy (39.2 +/- 5.3 mg/L), 2 women taking oral contraceptives (25.7 and 27.0 mg/L), and 3 women with acute hepatitis (34.8 +/- 4.8 mg/L) were associated with significant elevations of % peak A values (5.68 +/- 1.73%, 3.31% and 2.41%, and 3.25 +/- 0.78%, respectively) compared to those in normal subjects (1.33 +/- 0.40%), as well as increased anodal mobility on IEF. Treatment of a man for 3 days with ethinyl estradiol produced similar changes. Using data from densitometry measurements of IEF bands of TBG, the degree of anodal shift was quantitated (anodal index). This index correlated with the % peak A (r = 0.92) in all study subjects. We conclude that increased sites for sialylation, resulting from the increased proportions of triantennary oligosaccharide chains, account for the increased anodal mobility of TBG in hyperestrogenemia and hepatitis. Thus, in these two conditions, a reduced TBG degradation rate resulting from oligosaccharide modification is the likely mechanism of increased serum TBG levels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relationship of oligosaccharide modification to the cause of serum thyroxine-binding globulin excess. 312 46

To determine whether thyroid hormone-binding proteins in serum, particularly albumin, facilitate the transfer of T4 into human tissues, we studied cellular T4 uptake (CT4) by human liver (Hep G2) cells from medium containing serum from subjects with familial dysalbuminemic hyperthyroxinemia (FDH) and acquired and familial T4-binding globulin (TBG) excess and patients with normal T4-binding to albumin and normal TBG concentrations. Serum from nine subjects with FDH whose mean serum total T4 (TT4) concentration was 203 +/- 27 nmol/L were matched for TT4 concentrations with serum from nine subjects with acquired TBG excess (TT4, 201 +/- 23 nmol/L) and nine subjects with thyrotoxicosis and normal TBG concentrations (TT4, 205 +/- 28 nmol/L). The subjects' CT4 results were compared to their serum free T4 concentration, measured by equilibrium dialysis (DT4), and their serum free T4 index (FT4I) value. The mean serum DT4 value for the subjects with FDH (23 +/- 5 fmol/L) and those with TBG excess (23 +/- 3 fmol/L) were normal, whereas it was elevated (44 +/- 9 fmol/L; P less than 0.001) for the thyrotoxic patients with normal TBG concentrations. The mean CT4 value also was normal for the subjects with FDH (37.7 +/- 4.9 fmol/plate) and those with TBG excess (36.6 +/- 4.6 fmol/plate), but was elevated for the thyrotoxic patients (62.3 +/- 11.2 fmol/plate; P less than 0.001). In all three groups studied, the relationship between individual CT4 and DT4 values was similar to that previously found in subjects with no T4-binding protein abnormalities. The mean serum FT4I value was lower for the subjects with acquired TBG excess (111 +/- 22) than for the subjects with FDH (133 +/- 22; P less than 0.05), and it was much higher for the subjects with thyrotoxicosis (221 +/- 31; P less than 0.001). In the subjects with FDH and those with thyrotoxicosis the normal relationship between CT4 and FT4I was maintained, while in the subjects with acquired TBG excess, FT4I values were lower than expected. In seven of the nine subjects with TBG excess, the abnormality was associated with conditions known to increase its sialic acid content: hepatitis (one subject), pregnancy (four subjects), and estrogen therapy (two subjects). The CT4 values were similar in nine subjects with acquired TBG excess (seven pregnant women and two subjects with chronic active hepatitis) and five subjects with familial TBG excess (34.8 +/- 4.3 vs. 34.0 +/- 8.6 fmol/plate, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Normal cellular uptake of thyroxine from serum of patients with familial dysalbuminemic hyperthyroxinemia or elevated thyroxine-binding globulin. 314 12

The concentrations of triiodothyronine (T3), thyroxine (T4), T3/T4 ratio, free thyroxine index, and thyroxine-binding globulin were investigated in 114 viral hepatic disease patients and 36 controls. The T3/T4 ratio in healthy hepatitis B virus carriers was significantly greater than those in the controls and fulminant, acute, or chronic active hepatitis patients. The T3/T4 ratio in the fulminant hepatitis patients was significantly less than those in the controls and other liver disease patients. The correlation coefficient between the T3/T4 ratio and microsomal arylamidase activity in liver tissue from 30 patients was 0.78 (p less than 0.001). The correlation coefficient between the T3/T4 ratio and the content of cholinesterase was 0.64 (p less than 0.001). These results suggest that the T3/T4 ratio represents a marker of microsomal function and is useful for estimation of prognosis of fulminant hepatitis or differentiation of various viral hepatic diseases.
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PMID:Serum thyroid hormone, triiodothyronine, thyroxine, and triiodothyronine/thyroxine ratio in patients with fulminant, acute, and chronic hepatitis. 370 63

Two patients are presented who had unexpected increases in serum thyroxine concentration due to acquired thyroxine-binding globulin excess associated with asymptomatic hepatitis. Serum hormone concentrations were also analyzed retrospectively in 10 outpatients with viral hepatitis. Acute hepatitis is associated with an increase in serum thyroxine and thyroxine-binding globulin concentrations and a corresponding decrease in the triiodothyronine resin uptake. In five patients, serum thyroxine concentration (mean +/- SD) was elevated at 21.08 +/- 5.86 micrograms/dl during illness, and decreased to 10.18 +/- 2.96 micrograms/dl during full recovery (p less than 0.05); serum thyroxine-binding globulin concentration was elevated at 2.14 +/- 0.36 mg/dl during illness, and decreased to 1.18 +/- 0.16 mg/dl during recovery (p less than 0.01). Interpretation of thyroid function test results can be difficult in patients with hepatitis. When serum thyroxine is elevated, careful attention to a decrease in the triiodothyronine resin uptake is essential to avoid the incorrect diagnosis of hyperthyroidism. Occasionally, this change in the triiodothyronine resin uptake may be the first evidence of occult hepatic inflammation.
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PMID:Elevated thyroxine levels due to increased thyroxine-binding globulin in acute hepatitis. 640 65

Elevation of Thyroxine-binding globulin (TBG) in serum may lead to abnormally high total-thyroxine (T4) concentration. Causally hyper-TBG-aemia can either be acquired (estrogentherapy; hepatitis etc.) or familial. In a family-study with 3 generations 6 persons were found with this rare anomaly. Analysis of the pedigree is in accordance with an X-chromosomal transmission. Five of the affected family members were clinically euthyroid and had normal T4/TBG and effective thyroxine ratios (ETR). In one patient hypothyroidism was detected by these indirect parameters despite a normal T4-concentration. Changes in serum levels of thyroxine binding proteins make it difficult to diagnose a disturbance in thyroid function. However indirect parameters for free T4 (ETR, T4/TBG) as well as the TRH-Test allow a clear diagnosis in such patients.
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PMID:[Familial increase in thyroxine binding globulins in the blood]. 640 36

The liver has an important role in thyroid hormone metabolism and the level of thyroid hormones is also important to normal hepatic function and bilirubin metabolism. Besides the associations between thyroid and liver diseases of an autoimmune nature, such as that between primary biliary cirrhosis and hypothyroidism, thyroid diseases are frequently associated with liver injuries or biochemical test abnormalities. For example, thyroid diseases may be associated with elevation of alanine aminotransferase and alkaline phosphatase, which is mainly of bone origin, in hyperthyroidism and aspartate aminotransferase in hypothyroidism. Liver diseases are also frequently associated with thyroid test abnormalities or dysfunctions, particularly elevation of thyroxine-binding globulin and thyroxine. Hepatitis C virus infection has been connected with thyroid abnormalities. In addition, antithyroid drug therapy may result in hepatitis, cholestasis or transient subclinical hepatotoxicity, whereas interferon (IFN) therapy in liver diseases may also induce thyroid dysfunctions. These thyroid-liver associations may cause diagnostic confusions. Neglect of these facts may result in over of under diagnosis of associated liver or thyroid diseases and thereby cause errors in patient care. It is suggested to measure free thyroxine (FT4) and thyroid-stimulating hormone (TSH) which are usually normal in euthyroid patients with liver disease, to rule out or rule in coexistent thyroid dysfunctions, and consider the possibility of thyroid dysfunctions in any patients with unexplained liver biochemical test abnormalities. It is also advisable to monitor patients with autoimmune liver disease or those receiving IFN therapy for the development of thyroid dysfunctions, and patients receiving antithyroid therapy for the development of hepatic injuries.
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PMID:Clinical associations between thyroid and liver diseases. 754 16